The production of coordinated limb movements requires that the nervous system master redundancies at the muscle and joint levels. This mastery is presumably accomplished through the imposition of biomechanical and/or neurophysiological constraints, which effectively reduce the degrees of freedom of the limb. These constraints are likely to be altered by stroke induced brain injury resulting in discoordination of limb movement. Clinically, the recovery process from stroke is characterized by the emergence of stereotypic multi-joint movement patterns, which reflect a loss of independent joint control. These patterns, in conjunction with the applicant's recent isometric and flexion reflex studies, provide evidence for a loss of certain muscle coactivation and joint torque patterns in the impaired arm. Accordingly, discoordination in stroke may largely represent a manifestation of additional neural constraints on motor outflow (i.e., disturbances in movement execution). This view contrasts with recent studies, which have attributed trajectory abnormalities in hemiparetic stroke patients to deficits in higher level motor planning. The general aim of this proposal is therefore to elucidate the role of abnormal neural constraints in upper limb discoordination following hemiparetic stroke. The applicant proposes to study 30 hemiparetic stroke subjects to identify and quantify, under isometric conditions, abnormal neural constraints on voluntary torques in the impaired upper limb (Aim 1). This aim will be realized by using a 6 degree of freedom load cell to provide simultaneous measurements of elbow and shoulder torques. The applicant expects to see severe limitations in the ability of the hemiparetic subject to generate combined shoulder, abduction and elbow extension, while the ability to combine abduction with elbow flexion, or shoulder flexion/extension with elbow flexion/extension torques may be largely preserved. Subsequently, the contribution of the neural constraints identified in Aim I to trajectory disturbances in the impaired limb (Aim 2) will be elucidated. It is hypothesized that the torque constraints identified in Aim I represent the dominant mechanism underlying the spatial disturbances of movement initiation in hemiparetic stroke, while "higher order" planning, is largely intact. Accordingly, it is expected that with the limb passively supported in the horizontal plane, hemiparetic subjects will exhibit a relatively preserved ability to modulate joint torques in accordance with task requirements. In contrast, with the limb unsupported, a severe degradation in performance for tasks, which require the generation of joint torque combinations outside the available repertoire, is expected to be found. Finally, the applicant plans to investigate the role of spinal interneural circuits in creating abnormal neural constraints in stroke using a spinal cutaneous reflex, the flexion reflex (Aim 3). Preliminary results have shown a significant overlap in flexion reflex induced shoulder and elbow torque patterns with torque patterns measured during voluntary isometric conditions(Aim 1). This overlap does not exist in control subjects or in the unimpaired upper limb. This overlap does not exist is control subjects or in the unimpaired limb. This implicates involvement of spinal interneuronal circuits in the generation of abnormal neural constraints in the impaired upper limb.